Chapter 8 Cardiac Pathology Flashcards
What is the most common cause of Ischemic Heart Disease and what are the risk factors?
Atherosclerosis. Risk factors are similar to those of atherosclerosis; incidence increases with age
What is stable angina?
chest pain that arises with exertion or emotional distress, does not occur at rest
What is stable angina due to?
atherosclerosis of coronary arteries with >70% stenosis; decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion
What does stable angina represent?
reversible injury to myocytes ( no necrosis)
What is a hallmark sign of reversible cell damage?
cell swelling
How does stable angina present?
chest pain (lasting <20 min) that radiates to the left arm or jaw, diaphoresis, and shortness of breath.
What does EKG show with stable angina?
ST-segment depression due to subendocardial ischemia
What relieves stable angina?
Rest or nitroglycerin (decreases preload)
What is unstable angina?
chest pain that occurs at rest (still reversible)
What is unstable angina usually due to?
rupture of an atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of a coronary artery
What type of injury does unstable angina represent?
reversible
What does EKG show in unstable angina?
ST-depression
What relieves unstable angina?
nitro
What does unstable angina carry a high risk for?
progression to MI
What is Prinzmetal angina?
episodic chest pain unrelated to exertion
What is prinzmetal angina due to?
vasospasm of coronary artery (completely shuts it)
What type of injury does prinzmetal angina represent?
reversible
What does EKG show in prinzmetal angina?
ST segement elevation due to transmural ischemia
What relieves prinzmetal angina?
Nitro or Ca channel blockers.
What type of cell injury occurs in MI?
necrosis of myocytes which is irreversible
What is usually the cause of MI?
rupture of an atherosclerotic plaque with thrombosis and COMPLETE occlusion of a coronary artery
What are some other causes of MI? (3)
coronary artery vasospasm (due to prinzmetal angina or cocaine use)
Emboli
Vasculitis (Kawasaki disease)
What are the clinical features of an MI?
severe crushing chest pain (lasting >20 min) that radiates to left arm or jaw, diaphoresis, and dyspnea (due to pulmonary congestion)
How are each of the four chambers of the heart usually affected in an MI?
Infarction usually incolves the LV: RV,RA,LA are generally spared.
What does occlusion of the LAD lead to in MI?
infarction of the anterior wall and anterior septum of the LV; LAD is most commonly involved artery in MI
What does occlusion of the RCA cause in MI?
leads to infarction of the posterior wall, posterior septum, and papillary muscles of the LV: RCA is the second most commonly involved artery in MI
What does occlusion of the left circumflex artery cause in MI?
infarction of the lateral wall of the LV
What portions of the wall are damaged initially in MI and what does EKG show?
Initially subendocardial necrosis involving less than 50% of the wall leads to ST-depression
What portions of the wall become damages with continued ischemia in an MI and what EKG changes are seen?
transmural necrosis involving most of the myocardial wall causing ST-elevation on EKG
What two cardiac enzymes become elevated in MI?
Troponin I and CK-MB
Describe the time course and level of troponin I after an MI?
Troponin I is the most sensitive and specific marker for MI. levels rise 2-4 hours after infarction, peak at 24 hours, and return to normal by 7-10 days
describe the time course and level of CK-MB after an MI?
CK-MB is used for detecting reinfarction that occurs days after an initial MI. levels rise in 4-6 hours, peak at 24, and return to normal by 72.
Name 6 pharmacological treatments of MI
1 ASA and/or Heparin - limits thrombosis
2 Supplemental oxygen - minimizes ischemia
3 Nitrates - vasodilate veins and coronary arteries
4 BB slows HR, decreasing oxy demand and risk for arrhythmia
5 ACE-I decreases LV dilation
6 Fibrinolysis or angioplasty- opens blocked vessel
What does reperfusion of ireversibly damaged cells cause?
can result in calcium influx, leading to hypercontraction of myofibrils (Contraction band necrosis)
Describe reperfusion injury and how this would show up in labs?
Return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes. Cardiac enzymes would continue to rise even after opening blocked vessels.
What are the gross and microscopic changes and complications from 0-4 hours following an MI?
Gross- NONE
Microscopic - NONE
Complications- Cardiogenic shock (massive infarction), CHF, arrythmia
What are the gross and microscopic changes and complications from 4-24 hours following an MI?
Gross- Dark discoloration
microscopic - coagulative necrosis
complications- arrhythmia (if it doesnt happen by now it probably wont happen)
What are the gross and microscopic changes and complications from 1-3 days following an MI?
Gross- yellow pallor
microscopic- neutrophils
complications - fibrinous pericarditis (only with transmural injury); presents as chest pain with friction rub
What are the gross and microscopic changes and complications from 4-7 days following an MI?
Gross - yellow pallor
microscopic - macrophages
complications - this is the time when the wall is the weakest. rupture of ventricular free wall (leads to cardiac tamponade), interventricular septum (leads to shunt), or papillary muscle (leads to mitral insufficiency)
What are the gross and microscopic changes and complications from 1-3 weeks following an MI?
Gross - red border emerges as granulation tissue enters from edge of infarct.
microscopic - granulation tissue with plump fibroblasts, collagen, and BV
complications - none in chart
What are the gross and microscopic changes and complications in the months following an MI?
gross - white scar (weaker than healthy tissue)
microscopic - fibrosis
complications - aneurysm, mural thrombus, or Dressler syndrome
What is Dressler syndrome?
autoimmune pericarditis due to antigen exposure after an MI usually 6-8 weeks post infarct.
What is Sudden cardiac death? what usually causes it?
Unexpected death due to cardiac disease: occurs without symptoms or <1 hours after symptoms arise. usually due to fatal ventricular arrhythmia
What is the most common etiology of sudden cardiac death?
acute ischemia; 90% of patients have preexisting severe atherosclerosis.
What are some less common causes of sudden cardiac death?
mitral valve prolapse, cardiomyopathy, and cocaine abuse (vasospasm)
What is chronic ischemic heart disease? What does it progress to?
Poor myocardial function due to chronic ischemic damages (with or without infarction); progresses to CHF
What are 5 causes of left-sided heart failure?
1 ischemia
2 hypertension leads to concentric hypertrophy, thicker wall, more difficult to fill
3 dilated cardiomyopathy
4 MI
5 restrictive cardiomyopathy (cant fill heart appropriately)
What are clinical features of left sided heart failure due to?
decreased forward perfusion and pulmonary congestion.
What does pulmonary congestion lead to in left sided heart failure?
leads to pulmonary edema.
results in dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles. Small congested arteries may burst, leading to intraaleolar hemorrhage; marked by hemosiderin-laden macrophages (heart failure cells)
What is the consequence of decreased forward perfusion in left sided heart failure?
decreased flow to kidneys leads to activation of RAS system. Fluid retention exacerbates CHF
What is the mainstay of treatment for left sided heart failure?
ACE-I
What is the most common cause of right sided heart failure and what are two other causes?
most common is left sided heart failure. other important causes include left-to-right shunt and chronic lung disease (cor pulmonale) - develop hypoxia, vessels constrict, pulmonary pressure and resistance increase
What are clinical features of right sided heart failure due to?
congestion
What are the clinical features of right sided heart failure?
JVD
painful hepatospenlomegaly with characteristic ‘nutmeg’ liver; may lead to cardiac cirrhosis
dependent pitting edema due to increased hydrostatic pressure.
When do congenital heart defects arise and what percent of live births are they seen in? are they mainly sporadic or inherited?
Arise during embryogenesis (usually weeks 3-8); seen in 1% of live births, most are sporadic
What do congenital cardiac defects often result in?
Shunting between the left (systemic) and right (pulmonary) circulations
Describe how the reversal of a left to right shunt occurs?
increased flow through th epulmonary circulation results in hypertrophy of pulmonary vessels and pulmonary hypertension. Increased pulmonary resistance eventually results in reversal of shunt, leading to late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia and clubbing.
How do defects with right to left shunting present?
usually as cyanosis shortly after birth
What is a ventricular septal defect and what is it associated with?
Defect in the septum that divides the right and left ventricles. Most common congenital heart defect. associated with fetal alcohol syndrome.
What does a VSD result in? comment of the effects of the size of the defect.
a left to right shunt. The size of the defect determines the extent of the shunting and age at presentation. Small defects are often asymptomatic; large defects can lead to eisenmenger syndrome.
What does treatment of a VSD involve?
surgical closure; small defects may close spontaneously.
What is an atrial septal defect? what is the most common type?
defect in the septum that divides the right and left atria; most common type is ostium secundum (90%)
What is ostium primum associated with?
Down Syndrome